Effects of the pyriproxyfen and fenthion on the gonadal morphology of Nile tilapia (Oreochromis niloticus: Perciformes, Cichlidae).

Commercially available insecticides present acute toxicity to the health of fish and other aquatic organisms, which may impair the local aquaculture. This study evaluated the gonadal morphology of freshwater fish exposed to pyriproxyfen and fenthion. Forty-five juvenile male Nile tilapias (Oreochromis niloticus) were divided into control, pyriproxyfen-exposed (0.01 g/L), and fenthion-exposed (0.001 g/L) groups. They were evaluated in three moments (30, 60, and 90 days). The variables analyzed were the gonadosomatic index (GSI), weight to length ratio, seminiferous tubules morphometry (diameter and height), tissue damage, and immunohistochemical analysis for caspase-3, tumor necrosis factor alpha (TNF-α), and vascular endothelial growth factor (VEGF). Pyriproxyfen and fenthion injured the seminiferous tubule tissue, and the damage progressed according to the exposure time. In addition, the GSI gradually reduced over time in all groups compared with the first moment (30 days), while caspase-3, TNF-α, and VEGF values increased only in the fenthion-exposed group. Therefore, pyriproxyfen and fenthion changed the gonadal morphology of male Oreochromis niloticus, which may affect their reproduction in the wild or captivity.

Genomic comparisons between hepatocarcinogenic and non-hepatocarcinogenic organophosphate insecticides in the mouse liver.

Short-term biomarkers of toxicity have an increasingly important role in the screening and prioritization of new chemicals. In this study, we examined early indicators of liver toxicity for three reference organophosphate (OP) chemicals, which are among the most widely used insecticides in the world. The OP methidathion was previously shown to increase the incidence of liver toxicity, including hepatocellular tumors, in male mice. To provide insights into the adverse outcome pathway (AOP) that underlies these tumors, effects of methidathion in the male mouse liver were examined after 7 and 28 day exposures and compared to those of two other OPs that either do not increase (fenthion) or possibly suppress liver cancer (parathion) in mice. None of the chemicals caused increases in liver weight/body weight or histopathological changes in the liver. Parathion decreased liver cell proliferation after 7 and 28 days while the other chemicals had no effects. There was no evidence for hepatotoxicity in any of the treatment groups. Full-genome microarray analysis of the livers from the 7 and 28 day treatments demonstrated that methidathion and fenthion regulated a large number of overlapping genes, while parathion regulated a unique set of genes. Examination of cytochrome P450 enzyme activities and use of predictive gene expression biomarkers found no consistent evidence for activation of AhR, CAR, PXR, or PPARα. Parathion suppressed the male-specific gene expression pattern through STAT5b, similar to genetic and dietary conditions that decrease liver tumor incidence in mice. Overall, these findings indicate that methidathion causes liver cancer by a mechanism that does not involve common mechanisms of liver cancer induction.

The cytotoxicity and genotoxicity of single and combined fenthion and terbufos treatments in human liver cells and zebrafish embryos.

The mechanism of genotoxicity of the individual and combined pesticides of terbufos and fenthion were evaluated using HepG2 cells and zebrafish embryos. We determined genotoxicity by neutral comet assay and phosphorylation of H2AX (γH2AX), which indicated that cells treated with terbufos and/or fenthion caused DNA double-strand breaks (DSBs). The combination of these pesticides at the equimolar concentration (40 µM) exhibited less toxicity, genotoxicity, and did not impact DNA homologous recombination (HR) repair activity compare to terbufos or fenthion alone treatment. In HepG2 cells, terbufos, fenthion and their combination decreased only Xrcc2 expression (one of DNA HR repair genes). Moreover, the combined pesticides decreased Xrcc6 expression (one of DNA non-homologous end joining (NHEJ) repair genes). In addition, only terbufos or fenthion decreased XRCC2 protein expression, while Ku70 was impacted in all of the treated cells irrespective of up or down regulation. In zebrafish embryos, only fenthion impaired HR genes (Rad51 and Rad18) expression at 24 h. After 48 h exposure to pesticides, the combined pesticides elevated HR genes (Rad51 and Xrcc2) expression while terbufos or fenthion inhibited the expression of these four genes (Rad51, Rad18, Xrcc2, Xrcc6). In addition, the hatching rate of zebrafish embryos with fenthion or the combined pesticide at 72 hpf was significantly impaired. Collectively, terbufos and/or fenthion in combining caused DSBs in HepG2 cells and zebrafish embryos. Moreover, the specific mechanism of combined pesticide both HepG2 and zebrafish embryos revealed antagonism interaction.

The effect of acute organophosphate intoxication on female rat hippocampus cornu ammonis region pyramidal neuron numbers, biochemistry and morphology.

BACKGROUND: The most commonly used insecticides and pesticides worldwide are organophosphate compounds, chemicals that irreversibly inhibit the cholinesterase enzyme. Acute intoxication with cholinesterase inhibitors is known to cause permanent effects on both the human and rat brains. AIM: To investigate the effect of acute organophosphate intoxication on hippocampus morphology, biochemistry, and pyramidal neuron numbers in female rats. METHODS: Twenty-one rats were randomly divided into three groups. The control group received normal nutrition and underwent no procedures. The sham group received intraperitoneal physiological serum, while the experimental group received intraperitoneal 0.8 g/kg fenthion. Rats were sacrificed 24 h after these procedures. The brains were removed and divided in two halves medially, with one side being kept in 10% neutral formalin. After fixation procedures, tissues were embedded in blocks, sliced, and stained. A neuron count was then performed for the hippocampus. The other hippocampus was homogenized and used for biochemical procedures. RESULTS: Hippocampus sections from rats in the experimental group exhibited swelling and loss of shape in pyramidal cells, while no changes were observed in the control or sham groups. The number of neurons in the experimental group was lower than in the control and sham groups. Biochemical analysis revealed higher MDA and GSH values in the experimental group compared to the control and sham groups. CONCLUSION: Our results show increased apoptotic neurodegeneration of cells in the cornu ammonis region of the hippocampus and changes in biochemical values in rats with acute organophosphate exposure.

Acute renal involvement in organophosphate poisoning: histological and immunochemical investigations.

PURPOSE: Today, the long-term effects of partial exposure of cholinesterase on the kidney continue to be a research topic. In this study, we aimed to histopathologically investigate the possible effect of acute toxicity due to fenthion, an organophosphate (OP) compound, on the kidneys. METHODS: In all, 21 rats were randomly divided into three groups. Experimental group was each administered intraperitoneal 0.8 g/kg fenthion within physiologic serum. Sham group was only administered intraperitoneal physiologic serum. The control group continued normal nutrition with no procedure performed. After 24 h, all rats were sacrificed by cervical dislocation. Half of the recipient kidney tissues were examined histopathologically and the other half biochemically. RESULTS: No histopathological findings were found in the control group. Rats in the experimental group were observed to have epithelial cell disorganization in tubules, moderate epithelial cell loss, and degeneration. Again, expansion of tubules, vacuolization of tubular epithelial cells, and tubular structure approaching atrophy were observed, with cells approaching apoptosis and common hemorrhage noted although rats in the sham group were observed to have mild tubular degeneration. CONCLUSIONS: It should not be forgotten that one of the causes of systemic complaints linked to acute toxicity exposed to the OP compound of fenthion may be cellular injury to glomerular and tubular structures in the kidneys.

Evaluation of an acute oral gavage method for assessment of pesticide toxicity in terrestrial amphibians.

Development of an acute oral toxicity test with a terrestrial-phase amphibian was considered necessary to remove the uncertainty within the field of agrochemical risk assessments. The bullfrog (Lithobates catesbeianus) was selected for use as it is a representative of the family Ranidae and historically this species has been used as an amphibian test model species. Prior to definitive study, oral gavage methods were developed with fenthion and tetraethyl pyrophosphate. Dimethoate and malathion were subsequently tested with both male and female juvenile bullfrogs in comprehensive acute oral median lethal dose (LD50) studies. Juvenile bullfrogs were administered a single dose of the test article via oral gavage of a single gelatin capsule of dimethoate technical (dimethoate) or neat liquid Fyfanon® Technical (synonym malathion), returned to their respective aquaria, and monitored for survival for 14 d. The primary endpoint was mortality, whereas behavioral responses, food consumption, body weight, and snout-vent length (SVL) were used to evaluate indications of sublethal toxicity (secondary endpoints). Acute oral LD50 values (95% fiducial interval) for dimethoate were 1459 (1176-1810, males) and 1528 (1275-1831, females), and for malathion they were 1829 (1480-2259, males) and 1672 (1280-2183, females) mg active substance/kg body weight, respectively. Based on the results of these studies, the methodology for the acute oral gavage administration of test items to terrestrial-phase amphibians was demonstrated as being a practical method of providing data for risk assessments. Environ Toxicol Chem 2018;37:436-450. © 2017 SETAC.

DNA Damage in Wistar Rats Exposed to Organophosphate Pesticide Fenthion.

In the last several decades, exposure to pesticides has become a concern to environmental and human health. Many pesticides are environmentally persistent and are characterized by varying degrees of toxicity and adverse effects, including DNA damage. The present study was undertaken to evaluate the genotoxic potential of organophosphate pesticide fenthion in Wistar rats, as assessed by the comet assay. Adult male Wistar rats were treated with a solution of fenthion at a concentration of 40 mg/kg/day, administered intraperitoneally for 18 consecutive days. Rats were killed 24 hours after the last pesticide administration, and the comet assay was performed in peripheral blood cells. The comet assay results revealed that the damage index (19.29 ± 3.59 vs. 7.80 ± 2.25) and the damage frequency (17.00 ± 3.46 vs. 7.5 ± 2.46) found in fenthion-treated rats were significantly higher than those found in the control group (p = 0.001 and p = 0.0006, respectively). The results show that fenthion affects the DNA integrity of rat cells and may induce DNA damage in exposed organisms.

Genotoxicity assessment and oxidative stress responses in freshwater African catfish Clarias gariepinus exposed to fenthion formulations.

Fenthion is one of the most widely used organophosphate insecticides for the control of many varieties of pests in Nigeria. The genotoxic effect of the pesticide was evaluated in the blood erythrocytes of Clarias gariepinus using the micronucleus (MN) test. The oxidative stress parameters were also studied in the liver and gill tissues. Fish were exposed to 2.0, 4.0, and 8.0 mgL-1 of fenthion and sampling was done on days 1, 7, 14, 21 and after 7-day recovery. Micronuclei induction was highest (7.55) on day 14 at all concentrations in the peripheral blood cells. Oxidative stress was evidenced by increased lipid peroxidation (LPO). Maximum LPO values of 62.47% and 71.17% were observed in the gill and liver tissues respectively in C. gariepinus exposed to 8.0 mgL-1 concentration of fenthion. There were alterations in the values of reduced glutathione (GSH), glutathione reductase (GR), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) during the exposure and recovery periods. The 7-day recovery period was not adequate to eliminate fenthion-induced changes as LPO, CAT, and GR activity remain elevated. However, MN frequency and activity of SOD, GSH, and GPx (except at 8.0 mgL-1) recovered. The present findings give further credence on the integrated use of MN test and oxidative stress parameters in risk assessment of pollutants in aquatic ecosystem.

Subchronic Exposure to Fenthion Induces Hematological Changes in Liver Tissue of African Catfish Clarias gariepinus.

In this study, African Catfish (also known as Sharptooth Catfish) Clarias gariepinus were exposed to sublethal concentrations of fenthion of 2.0, 4.0, and 8.0 mg/L for 21 d and allowed to recover for 7 d to investigate the potential for hematological changes. Whole blood was sampled on days 1, 7, 14, and 21 postexposure and after a 7-d recovery period. During exposure, fenthion caused a reduction in red blood cell counts, hemoglobin concentration, and packed cell volume. There was an increase in white blood cell counts but no significant difference in mean corpuscular hemoglobin concentration, mean corpuscular volume, and mean corpuscular hemoglobin. Both increases and decreases were observed in white blood cell differentials. After the 7-d recovery period, both increases and decreases were observed in the hematological parameters. These results reveal that sublethal concentrations of fenthion can cause hematological alterations in African Catfish and that the substance should be used with caution. Received October 20, 2015; accepted May 4, 2016.

Fenthion, an organophosphorus pesticide, induces alterations in oxidant/antioxidant status and histopathological disorders in cerebrum and cerebellum of suckling rats.

Fenthion (FEN) is an organophosphorus pesticide known for its wide toxic manifestations. In this study, the effects of FEN were evaluated on the cerebrum and cerebellum oxidant/antioxidant status and histopathological disorders in the suckling rats. Pregnant rats were divided into two groups: control group received pure water, while FEN group received daily by their drinking water 551 ppm of FEN from the 14th day of pregnancy until day 14 after delivery. Acetylcholine esterase (AChE) activity was inhibited in both the cerebrum and cerebellum of suckling rats whose mothers were treated with FEN. The cerebrum and cerebellum oxidative damage was demonstrated by a significant increase of malondialdehyde (MDA), advanced oxidation protein product and glutathione (GSH) levels and disturbance in the antioxidant enzyme activities. A significant decline of non-protein thiol and vitamin C levels was also observed. These changes were confirmed by histopathological observations which were marked by pyknotic neurons in the cerebrum and apoptotic cells in the cerebellum of FEN-treated rats. In the cerebellum of FEN-treated rats, the most conspicuous damage was the absence of external granular layer, indicating growth retardation. These data suggested that exposure of pregnant and lactating rats to FEN induced oxidative stress and histopathological disorders in the cerebrum and cerebellum of their pups. Thus, the use of FEN must be under strict control, especially for pregnant and lactating mothers.

Piperonyl butoxide increases oxidative toxicity of fenthion in the brain of Oreochromis niloticus.

The present study was designed to understand the effects of piperonyl butoxide (PBO), modulator of cytochrome P450 (CYP 450), on the neurotoxicity of organophosphate pesticide fenthion in the brain of Oreochromis niloticus used as a model organism. Fish were exposed to one-fourth of the LC50 value of fenthion (0.567 mg/L) and 0.5 mg/L PBO concentration for 24 h, 96 h, and 15 days. Glutathione (GSH)-related antioxidant system, lipid peroxidation, stress proteins, and acetylcholinesterase (AchE) activity were investigated. Our results showed that PBO induced the neurotoxic effect of fenthion with increasing oxidative stress in long-term exposure. GSH-related antioxidant system might take a role in protecting the brain from these oxidative effects. PBO possibly inhibited the biotransformation of fenthion by inhibiting CYP 450; thereby preventing the brain from AChE inhibition in short-term exposure. Changes in parameters indicated that PBO caused biphasic response by affecting CYP 450 in the brain of O. niloticus.

Protective effects of Artemisia campestris upon fenthion-induced nephrotoxicity in adult rats and their progeny.

The purpose of this study was to assess the possible protective effects of Artemisia campestris against fenthion-induced nephrotoxicity in adult rats and their progeny. Fenthion was administered orally at a dose of 551 ppm, which represented » of LD50, for 21 consecutive days to pregnant and lactating rats. Oxidative stress was monitored in the kidney by measuring malondialdehyde (MDA), GSH levels, catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase activities (GPx). Fenthion caused a significant induction of oxidative damage in kidney as evidenced by increased MDA levels from 5.32 ± 0.47 nmol/100 mg tissue to 11.72 ± 0.83 nmol/100 mg tissue for pups and from 5.18 ± 0.45 nmol/100 mg tissue to 10.84 ± 1.67 nmol/100 mg tissue for dams (p < 0.001). A significant increase (p < 0.001) in the activities of SOD, CAT and GPx was observed. Co-administration of Artemisia c. at a dose of 5% (w/w) in the diet of fenthion-treated rats showed a significant reno-protection against fenthion-induced cytotoxic effects. It could be concluded that Artemisia c. is promising as a protective agent against nephrotoxicity during the exposure to fenthion.

Effects of the organophosphate fenthion for control of the red-billed quelea Quelea quelea on cholinesterase and haemoglobin concentrations in the blood of target and non-target birds.

The red-billed quelea bird Quelea quelea is one of sub-Saharan Africa's most damaging pests, attacking small-grain crops throughout semi-arid zones. It is routinely controlled by spraying its breeding colonies and roosts with organophosphate pesticides, actions often associated with detrimental effects on non-target organisms. Attributions of mortality and morbidity of non-targets to the sprays are difficult to confirm unequivocally but can be achieved by assessing depressions in cholinesterase activities since these are reduced by exposure to organophosphates. Here we report on surveys of birds caught before and after sprays that were examined for their blood cholinesterase activities to assess the extent to which these became depressed. Blood samples from birds were taken before and after sprays with fenthion against red-billed quelea in colonies or roosts, and at other unsprayed sites, in Botswana and Tanzania and analysed for levels of haemoglobin (Hb) and activities of whole blood acetylcholinesterase (AChE) and butyrylcholinesterase (BChE). Background activities of AChE, BChE and Hb concentrations varied with bird species, subspecies, mass, age and gender. Contrary to expectation, since avian erythrocytes are often reported to lack cholinesterases, acetylcholinesterase activities in pre-spray samples of adult birds were positively correlated with Hb concentrations. When these factors were taken into account there were highly significant declines (P < 0.0001) in AChE and BChE and increases in Hb after contact with fenthion in both target and non-target birds. BChE generally declined further (up to 87 % depression) from baseline levels than AChE (up to 83 % depression) but did so at a slower rate in a sample of quelea nestlings. Baseline activities of AChE and BChE and levels of Hb were higher in the East African subspecies of the red-billed quelea Q. q. aethiopica than in the southern African subspecies Q. q. lathamii, with the exception of BChE activities for adult males which were equivalent.

Acute effects of fenthion on certain oxidative stress biomarkers in various tissues of frogs (Rana ridibunda).

This study was aimed mainly to assess the effects of fenthion on certain oxidative stress biomarkers in various tissues of frogs (Rana ridibunda). Biomarkers selected for stress monitoring were malondialdehyde (MDA) and antioxidant defense system (ADS) such as reduced glutathione (GSH) level, glutathione peroxidase (GSH-Px), glutathione-S-transferase (GST), and superoxide dismutase (SOD) activities in the liver, kidney, heart, and brain of frogs exposed to 10 and 20 ppm dosages of fenthion for 24, 48, 72, and 96 h. The results demonstrate an increase in MDA levels in selected tissues following exposure to both concentrations of fenthion. The ADS, GSH-Px, GST, SOD activities and GSH levels also fluctuated after 24, 48, 72, and 96 h in all the treatment groups compared with controls. From the evidence obtained here, it is concluded that the exposure of frogs to fenthion induced an increase in MDA combined with fluctuated ADS. This may reflect the potential role of these parameters as useful biomarkers for oxidative stress in amphibian species.

Fenthion and terbufos induce DNA damage, the expression of tumor-related genes, and apoptosis in HEPG2 cells.

This study investigates the effects of fenthion and terbufos, two organophosphorous pesticides, on DNA damage, tumor-related gene expression, and apoptosis in HepG2 cells. We found that exposure to concentrations ranging from 50 to 200 µM of fenthion and terbufos for 2 hr caused significant death in HepG2 cells. Both compounds induced DNA damage in a concentration-dependent manner as measured using the alkaline comet assay. Tumor-related genes (jun, myc, and fos) and apoptosis-related genes (socs3, tnfaip3, ppp1r15a, and nr4a1) were up-regulated by both compounds. Finally, both compounds induced apoptosis. The results demonstrate that both terbufos and fenthion induce DNA damage and should be considered potentially hazardous to humans.

Neurotoxic and immunotoxic effects of fenthion and omethoate on frogs at acute exposure.

The study was carried out to investigate the neurotoxic and immunotoxic effects of fenthion- and omethoate-used agricultural areas on frogs (Rana ridibunda) at acute exposure. The neurotoxic effects of the chemicals were evaluated by measuring the activities of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE). Biomarkers selected for immunotoxic monitoring were the activities of adenosine deaminase (ADA) and myeloperoxidase (MPO) in various tissues of frogs exposed to 10 or 20 parts per million (ppm) dosages of fenthion and omethoate for 24, 48, 72 and 96 hours. Results showed that the administrations of chemicals fluctuated AChE and BChE activities in some tissues of frogs treated with both dosages at all the periods. With regard to the immunotoxic effects, MPO activity was increased in almost all the tissues of frogs after 10 and 20 ppm dosages and for 24, 48, 72 and 96 hours exposure of fenthion and omethoate as compared to those of control whereas ADA activity did not change in all the tissues. This may reflect the potential role of these parameters as useful biomarkers for toxicity of fenthion and omethoate.

Combination larvicidal action of Solanum xanthocarpum extract and certain synthetic insecticides against filarial vector, Culex quinquefasciatus (SAY).

The combination activities of temephos, fenthion and petroleum ether extract of Solanum xanthocarpum were observed for their larvicidal activities against Culex quinquefasciatus. The combination of temephos and S. xanthocarpum was studied at ratios of 1:1, 1:2, and 1:4. Similar ratios were also used for the combination of fenthion and S. xanthocarpum. The temephos/plant extract combination acted antagonistically. The combination of fenthion and plant extract acted synergistically against the target organisms at a ratio of 1:1, which showed the best results of: LC50 0.0144 and 0.0056 ppm and LC90 0.0958 and 0.0209 ppm at 24 and 48 hours, respectively. The present study will be helpful in developing a commercial formulation for effective vector management.

Tissue-specific effects of fenthion on glutathione metabolism modulated by NAC and BSO in Oreochromis niloticus.

INTRODUCTION: The present study was designed to understand the effects of organophosphate (OP) insecticide and avicide fenthion on cellular redox status and the role of reduced glutathione (GSH) on fenthion toxicity in the liver and kidney of Oreochromis niloticus as a model organism. N-acetylcysteine (NAC) and buthionine sulfoximine (BSO) were injected intraperitoneally to fenthion-exposed fish as modulators of GSH metabolism. GSH redox status, GSH-related enzyme activities, and thiobarbituric acid reactive substances (TBARS) contents were then measured spectrophotometrically at 24, 48, and 96 hours. To assess recovery from fenthion exposure, similar analyses were performed on fish transferred to non-treated water for 24, 48, and 96 hours. RESULTS: Fenthion increased glutathione S-transferase (GST; EC 2.5.1.18) activity and caused changes in total GSH (tGSH), GSH and oxidized glutathione (GSSG) contents and glutathione peroxidase (GPx; EC 1.11.1.9) specific activity in the liver tissue over time. Increases observed in tGSH and GSSG contents at 24 hours were decreased by fenthion treatment at 96 hours. BSO caused a sharp decline in liver tGSH, GSH, and GSSG contents and an elevation in GST and gamma-glutamyl transpeptidase (gamma-GT; EC 2.3.2.2) enzyme activities. A significant decrease was observed in tGSH and GSH contents and, also, GST enzyme activities in the kidney at 48-hour fenthion treatment. On the contrary to the liver, a significant increase was observed in tGSH and GSH contents in the kidney by BSO injection. NAC application eliminated the decreasing effects of fenthion on GST activity in this tissue. NAC injection caused decreases in lipid peroxidation (LPO) levels. Decline in tGSH and GSH contents were maintained in the liver during the recovery period, and elevations in LPO levels in the kidney were observed during the same period. CONCLUSIONS: In conclusion, tissue-specific and time-dependent GSH redox status disturbance of fenthion were observed. BSO revealed the significance of GST-mediated GSH conjugation on the detoxification process of fenthion. NAC seemed useful to avoid the fenthion-related oxidative toxicity.

Tissue trace and major element levels in organophosphate insecticide fenthion (Lebaycid) toxicity in rats: prophylactic and therapeutic effect of exogenous melatonin.

Organophosphate compounds are very toxic chemicals and used in widespread applications. The present study was designed to examine the role of exogenous melatonin against organophosphate toxicity in tissues (brain, heart, jejunum, kidney, liver, lung, muscle and pancreas) trace and major element levels of rats. Trace and major element concentrations in the tissues were measured in the sham group, the control group, prophylaxis with the melatonin group and therapy with the melatonin group (TM) by inductively coupled plasma-optical emission spectroscopy. Statistically significant differences among the experimental groups were detected for some tissue trace and major element concentrations. In the brain tissue, the Al, Mn and Se concentrations in the sham group were significantly higher than those in the control group (p<0.05). In the heart tissue, the Cu, Mn and Se concentrations in the sham group were significantly increased than those in the control group (p<0.05). In the kidney tissue, trace and major element concentrations in the TM group were significantly lower than those in the sham group (Fe and Mn; p<0.05, Cu, Mo, Ni, Ti, V and Zn; p<0.01). In the liver, Mg, Al, Zn and Ca concentrations in the TM group were significantly higher than those in the fenthion-treated control group (p<0.01). In the muscle tissue, element concentrations in the TM group were significantly lower when compared with the sham groups (Ca and Si; p<0.01). The Al, Cr, Mo, Ni, Si and Zn element concentrations were markedly decreased in the control group as compared with the TM group in the pancreas tissue (p<0.01). In conclusion, according to the results of the present study the major findings are that the fenthion-treated rat's tissue element levels were effected and the melatonin may normalize the altered levels of some trace and major elements of the tissues in organophosphate toxicity.

Tissue-specific in vivo inhibition of cholinesterases by the organophosphate fenthion in Oreochromis niloticus.

This study was designed to elucidate the effect of the organophosphate fenthion exposure on cholinesterase-specific activities in brain, liver, and kidney tissues of juvenile Oreochromis niloticus, and to define the best indicator tissue to fenthion exposure. The 96-h LC(50) value was determined as 2.27 mg/L and fish were exposed to 20% of this concentration for 24-, 48-, and 96-h. Recovery periods in similar durations were provided to evaluate the ChE activities. AChE and BChE activities were determined spectrophotometrically. The activities of these enzymes were significantly inhibited in all the tissues tested, liver was the most and kidney was the least affected tissues. The inhibition percentages of AChE and BChE were at similar levels in the liver while BChE was more affected in kidney. BChE was not detected in the brain. A significant positive correlation in ChE inhibitions was found among tissues, and the effect of fenthion on ChE activities was tissue specific. In general enzymes activities were not significantly recovered in 96-h recovery period; however, an elevation in AChE inhibition was observed in brain. Based on the data of this study, the liver may be suggested as the best indicator tissue especially for phosphorothioate exposure.